• 제목/요약/키워드: Virus Latency

검색결과 16건 처리시간 0.026초

A Restrictive Virus Tropism, Latency and Reactivation of Pseudorabies Virus Following Irreversible Deletion of Bsrl Restriction Site in the Thymidine-kinase Gene

  • Mohd Lila Mohd Azmi;Zeenathul, Nazariah-Allaudin;Abdel-Wahid Saeed Ali;Che Abdul Rahim Mohamed;Kamarudin, Awag-Isa
    • Journal of Microbiology
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    • 제40권1호
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    • pp.1-10
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    • 2002
  • At the dose of 1000 p.f.u. per mouse,100% mortality occurred in mice inoculated with wild-type pseudorabies virus (PrV). In contrast, upon stable deletion of 10 bp nucleotides at the Bsrl site within the TK gene, PrV was rendered to be completely apathogenic. The deletion also caused the virus to be less capable of replicating in respiratory as well as in nervous system tissues. Although animals were exposed to high titers of TK-deleted PrVs, the virus failed to replicate to a high titer as compared to the pathogenic parental virus. In contrast to previous studies the deletion in the TK gene did not prevent the virus from establishing latency. Upon immunosuppression, the latent virus? however, reactivated but replicated at low titers. Interestingly, TK-deleted virus established latency and reactivation, that are occurred only in trigeminal ganglia and the cerebrums and no other tissues involved. Following reactivation, there was no indication of virus shedding in respiratory tissues as confirmed by virus isolation and polymerase chain reaction (PCR) technique targeting at the gB gene of PrV, The non-pathogenic virus with non-shedding characteristics, upon reactivation of the latent virus, would be the important feature of a live virus vaccine candidate.

Common viral infections in kidney transplant recipients

  • Vanichanan, Jakapat;Udomkarnjananun, Suwasin;Avihingsanon, Yingyos;Jutivorakool, Kamonwan
    • Kidney Research and Clinical Practice
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    • 제37권4호
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    • pp.323-337
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    • 2018
  • Infectious complications have been considered as a major cause of morbidity and mortality after kidney transplantation, especially in the Asian population. Therefore, prevention, early detection, and prompt treatment of such infections are crucial in kidney transplant recipients. Among all infectious complications, viruses are considered to be the most common agents because of their abundance, infectivity, and latency ability. Herpes simplex virus, varicella zoster virus, Epstein-Barr virus, cytomegalovirus, hepatitis B virus, BK polyomavirus, and adenovirus are well-known etiologic agents of viral infections in kidney transplant patients worldwide because of their wide range of distribution. As DNA viruses, they are able to reactivate after affected patients receive immunosuppressive agents. These DNA viruses can cause systemic diseases or allograft dysfunction, especially in the first six months after transplantation. Pretransplant evaluation and immunization as well as appropriate prophylaxis and preemptive approaches after transplant have been established in the guidelines and are used effectively to reduce the incidence of these viral infections. This review will describe the etiology, diagnosis, prevention, and treatment of viral infections that commonly affect kidney transplant recipients.

Herpes Simplex Virus Type 1 마우스 뇌염모델에서의 조직내 바이러스 증식 및 재활성에 미치는 Acyclovir의 약효 (Efficacy of Acyclovir on Virus Replication in Infected Tissues and Virus Reactivation from Explanted Tissues in Mouse Encephalitis Model of Herpes Simplex Virus Type 1)

  • 이종교;김지현;배판기;피미경;김해수
    • 대한바이러스학회지
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    • 제29권3호
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    • pp.165-174
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    • 1999
  • To investigate viral pathogenesis and in vivo efficacy of acyclovir (ACV) in mouse HSV-1 encephalitis models, female BALB/c mice aged 5 weeks were inoculated with strain F either intranasally (IN) or intracerebrally (IC). ACV-treatment by intraperitomeal injection with 0, 5, 10 and 25 mg/kg b.i.d. for 6 days was commenced 1 h after infection. Body weight and signs of clinical disease were noted daily up to 2 weeks. $ED_{50}$ of ACV in IN infection was <5 mg/kg and 14.1 mg/kg in IC infection. Tissues of central nervous system were collected from 2 mice per group everyday up to 5 day p.i. and the virus titers were measured. In IN infection model, high titers in eyes and trigeminal nerves were observed. ACV-treatment showed significant reduction of the titers in all the isolated. In IC infection model, cerebrum, cerebellum and brain stem showed high virus titers. ACV-treatment showed less significant reduction of virus titers than that in IN infection model. Reactivation of explanted trigeminal nerves from mice 30 day p.i. was monitored. In all of ACV treated mice reactivation was observed, i.e. even the highest dose of ACV did not inhibit the establishment of viral latency.

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Investigation of functional roles of transcription termination factor-1 (TTF-I) in HIV-1 replication

  • Park, Seong-Hyun;Yu, Kyung-Lee;Jung, Yu-Mi;Lee, Seong-Deok;Kim, Min-Jeong;You, Ji-Chang
    • BMB Reports
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    • 제51권7호
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    • pp.338-343
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    • 2018
  • Transcription termination factor-1 (TTF-I) is an RNA polymerase 1-mediated transcription terminator and consisting of a C-terminal DNA-binding domain, central domain, and N-terminal regulatory domain. This protein binds to a so-called 'Sal box' composed of an 11-base pair motif. The interaction of TTF-I with the 'Sal box' is important for many cellular events, including efficient termination of RNA polymerase-1 activity involved in pre-rRNA synthesis and formation of a chromatin loop. To further understand the role of TTF-I in human immunodeficiency virus (HIV)-I virus production, we generated various TTF-I mutant forms. Through a series of studies of the over-expression of TTF-I and its derivatives along with co-transfection with either proviral DNA or HIV-I long terminal repeat (LTR)-driven reporter vectors, we determined that wild-type TTF-I downregulates HIV-I LTR activity and virus production, while the TTF-I Myb-like domain alone upregulated virus production, suggesting that wild-type TTF-I inhibits virus production and trans-activation of the LTR sequence; the Myb-like domain of TTF-I increased virus production and trans-activated LTR activity.

마렉병 바이러스 감염과 병원성 발현 기전 (Infection and Pathogenesis Mechanisms of Marek's Disease Virus)

  • 장형관;박영명;차세연;박종범
    • 한국가금학회지
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    • 제35권1호
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    • pp.39-55
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    • 2008
  • Like the other herpesviruses, the virion of MDV consists of an envelope, which surrounds an amorphous tegument. Within the tegument, and icosahedral capsid encloses a linear double-stranded DNA core. Although the genome structure of MDV indicates that it is an ${\alpha}-herpesvirus$ like herpes simplex and varicella-zoster viruses, biological properties indicate MDV is more akin to the ${\gamma}-herpesvirus$ group, which includes Epstein-Barr and Kaposi's sarcoma herpesviruses. These herpesviruses replicate lytically in lymphocytes, epithelial and fibroblastic cells, and persist in lymphoblastoid cells. MDV has a complex life cycle and uses two means of replication, productive and non-productive, to exist and propagate. The method of reproduction changes according to a defined pattern depending on changes in virus-cell interactions at different stages of the disease, and in different tissues. Productive (lytic) interactions involve active invasion and take-over of the host cell, resulting in the production of infectious progeny virions. However, some herpesviruses, including MDV, can also establish a non-productive (abortive) infection in certain cell types, resulting in production of cell-associated progeny virus. Non-productive interactions represent persistent infection, in which the viral genome is present but gene expression is limited, there is no structural or regulatory gene translation, no replication, no release of progeny virions and no cell death. Reactivation of the virus is rare, and usually the infectious virus can be re-isolated only after cultivation in vitro. MDV establishes latency in lymphoid cells, some of which are subsequently transformed. In this review article, recent knowledges of the pathogenesis mechanisms followed by MDV infection to sensitive cells and chickens are discussed precisely.

다발성 하부뇌신경을 침범한 대상포진 감염 치험 1례 (A Case of Varicella-Zoster virus infection with multiple cranial nerve involvement)

  • 신정은;유증주;김상윤;남순열
    • 대한기관식도과학회지
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    • 제5권2호
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    • pp.222-230
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    • 1999
  • Varicella-zoster virus(VZV) becomes latent in the sensory ganglia after primary infection and emerges from latency to cause zoster in adults. After primary infection, VZV remains latent in the dorsal spinal ganglia. The mechanisms responsible for its reactivation and the clinical entity of herpes zoster are poorly understood. Reactivation of VZV is commonly known to manifest as Ramsay Hunt syndrome which is one of the VZV-associated neurologic diseases with facial paralysis, ear pain, and a characteristic herpetic auricular rash. It is now known that lesions of this syndrome can affect all cranial nerves. Central, cervical and peripheral effects of this syndrome is polyneuropathic in nature. VZV usually involves the 5th and 7th cranial nerves and less commonly the lower cranial nerves such as 9th and 10th. We report a treated case of healthy 40 years old male with VZV infection of the 5th, 9th and 10th cranial nerves. The patient typically showed herpetic vesicles in the auricle and temporal bone area without facial paralysis.

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Electroacupuncture Analgesia Is Improved by Adenoviral Gene Transfer of Dopamine Beta-hydroxylase into the Hypothalamus of Rats

  • Kim, Soo-Jeong;Chung, Eun Sook;Lee, Jun-Ho;Lee, Chang Hoon;Kim, Sun Kwang;Lee, Hye-Jung;Bae, Hyunsu
    • The Korean Journal of Physiology and Pharmacology
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    • 제17권6호
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    • pp.505-510
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    • 2013
  • Electroacupuncture (EA) is a modified form of acupuncture that utilizes electrical stimulation. We previously showed that EA stimulated rats were divided into responders that were sensitive to EA and non-responders that were insensitive to EA based on the tail flick latency (TFL) test. The dopamine beta-hydroxylase (DBH) gene was more abundantly expressed in the hypothalamus of responder rats than non-responder rats. To determine whether overexpression of DBH gene expression in the hypothalamus modulate EA analgesia, we constructed a DBH encoding adenovirus and which was then injected into the hypothalamus of SD rats. Microinjection of DBH or control GFP virus into the hypothalamus had no changes on the basal pain threshold measured by a TFL test without EA treatment. However, the analgesic effect of EA was significantly enhanced from seven days after microinjection of the DBH virus, but not after injection of the control GFP virus. DBH expression was significantly higher in the hypothalamus of DBH virus injected rat than control GFP virus or PBS injected rats. Moreover, expression of the DBH gene did not affect the body core temperature, body weight, motor function or learning and memory ability. Although the functional role of DBH in the hypothalamus in the analgesic effect of EA remains unclear, our findings suggest that expression of the DBH gene in the hypothalamus promotes EA analgesia without obvious side-effects.

건강한 어린 소아에서 수두 백신 접종 후 발생한 대상포진 2예: 백신주에 의한 1예 (Two Cases of Herpes Zoster Following Varicella Vaccination in Immunocompetent Young Children: One Case Caused by Vaccine-Strain)

  • 김다은;강혜지;한명국;염혜영;장성희
    • Pediatric Infection and Vaccine
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    • 제29권2호
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    • pp.110-117
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    • 2022
  • 대상포진은 소아에서 흔하지 않은 질환이며, 국외의 자료에서는 수두 백신 접종 정책 시행 후 대상포진의 발생률이 감소되었다. 저자들은 건강한 어린 소아에서 수두 백신 접종 후 발생한 대상포진 2예를 경험하였다. 특히 이중 1예에서는 피부 검체를 검사하여 대상포진이 백신주 varicella-zoster virus (VZV)에 의한 것을 확인하였다. 2예 모두 발진이 번지는 양상이어서 항바이러스제를 투여하였고 호전되었다. 수두 백신을 접종 받은 어린 소아가, 수두에 이환 되거나 노출된 적이 없으며, 대상포진이 발병하였을 경우 백신주에 의한 대상포진의 가능성을 고려해야 한다.

후두암종에서 Ebstein-Barr 바이러스 DNA와 Bcl-2 단백의 검색 (Detection of Ebstein-Barr Virus DNA and Bcl-2 Protein in Laryngeal Squamous Cell Carcinoma)

  • 이상숙;박남조;박준식
    • 대한두경부종양학회지
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    • 제16권1호
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    • pp.14-19
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    • 2000
  • Objectives: Epstein-Barr virus(EBV) is a B-lymphotrophic virus with a tumorigenic potential. EBV infection has been recognized as the main cause of nasopharyngeal carcinoma and Burkitt's lymphoma. Bcl-2 protein expression is known to be up-regulated by the EBV-latency associated antigen latent membrane protein(LMP). The aim of this study was to determine the incidence of EBV in squamous cell carcinomas of the larynx and the relationship between the presence of EBV and bcl-2 expression. Patients and Methods: From January 1994 to December 1977, 35 patients with primary squamous cell carcinoma of the larynx were studied. EBV genome DNA was surveyed by polymerase chain reaction(PCR) assay and then compared the results of in situ hybridization(ISH) for EBER1 using digoxigenin-tailed oligonucleotide probe. The expression of bcl-2 protein was studied by immunohistochemistry(IHC) using bcl-2 monoclonal antibody. Results: By PCR, EBV genome was detected in 22 of 35(62.9%) squamous cell carcinomas of the larynx. Nineteen of 35 cases(54.3%) showed a positive nuclear staining for EBER1 in tumor cells by ISH. Three cases showed positivity in inflammatory cells by ISH and one of them showed a positive staining of both tumor cells and inflammatory cells. Eighteen of 32 specimens(62.5%) were positive for bcl-2 protein. There was no significant correlations between the presence of EBV DNA and bcl-2 expression. Conclusions: It could be concluded that high incidence of EBV in the laryngeal cancer tissue may indicate a probable role of EBV in the development of laryngeal carcinoma.

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바이러스 감염에 대한 면역반응 (Immune Responses to Viral Infection)

  • 황응수;박정규;차창용
    • IMMUNE NETWORK
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    • 제4권2호
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    • pp.73-80
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    • 2004
  • Viruses are obligate intracellular parasites which cause infection by invading and replicating within cells. The immune system has mechanisms which can attack the virus in extracellular and intracellular phase of life cycle, and which involve both non-specific and specific effectors. The survival of viruses depends on the survival of their hosts, and therefore the immune system and viruses have evolved together. Immune responses to viral infection may be variable depending on the site of infection, the mechanism of cell-to-cell spread of virus, physiology of the host, host genetic variation, and environmental condition. Viral infection of cells directly stimulates the production of interferons and they induce antiviral state in the surrounding cells. Complement system is also involved in the elimination of viruses and establishes the first line of defence with other non-specific immunity. During the course of viral infection, antibody is most effective at an early stage, especially before the virus enters its target cells. The virus- specific cytotoxic T lymphocytes are the principal effector cells in clearing established viral infections. But many viruses have resistant mechanism to host immune responses in every step of viral infection to cells. Some viruses have immune evasion mechanism and establish latency or persistency indefinitely. Furthermore antibodies to some viruses can enhance the disease by the second infection. Immune responses to viral infection are very different from those to bacterial infection.